GTP cyclohydrolase I/BH4 pathway protects EPCs via suppressing oxidative stress and thrombospondin-1 in salt-sensitive hypertension.

Journal article

Endothelial progenitor cells (EPCs) are both reduced and dysfunctional in hypertension that correlates inversely with its mortality, but the mechanisms are poorly understood. Endothelial nitric oxide synthase (eNOS) critically regulates EPC mobilization and function but is uncoupled in salt-sensitive hypertension because of the reduced cofactor tetrahydrobiopterin (BH4). We tested the hypothesis that GTP cyclohydrolase I (GTPCH I), the rate-limiting enzyme of BH4 de novo synthesis, protects E...

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Authors: Xie, H; Zhou, S; Chen, D; Channon, K; Su, D

• Publication status: Published
• Journal: Hypertension
• Volume: 56
• Issue: 6
• Pages: 1137-1144
• Publication date: 2010-12-01
• DOI: 10.1161/hypertensionaha.110.160622
• EISSN: 1524-4563
• ISSN: 0194-911X
• Language: English
• Keywords: Biopterin; Cell Adhesion; GTP Cyclohydrolase; Nitroarginine; Nitric Oxide; Superoxides; Thrombospondin 1; Polyethylene Glycols; Male; Desoxycorticosterone; Hypertension; Stem Cells; Nitric Oxide Synthase Type III; Superoxide Dismutase; Oxidative Stress; Mice, Inbred C57BL; Angiogenesis Inhibitors; Neovascularization, Physiologic; Mice; Mice, Transgenic; Animals